PUBLICATION
Carnosic acid attenuates acrylamide-induced retinal toxicity in zebrafish embryos
- Authors
- Albalawi, A., Hasaballah A Alhasani, R., Biswas, L., Reilly, J., Akhtar, S., Shu, X.
- ID
- ZDB-PUB-180622-44
- Date
- 2018
- Source
- Experimental Eye Research 175: 103-114 (Journal)
- Registered Authors
- Keywords
- Acrylamide, Carnosic acid, Oxidative damage, Retina, Zebrafish
- MeSH Terms
-
- Abietanes/pharmacology*
- Acrylamide/toxicity*
- Animals
- Antioxidants/pharmacology*
- Catalase/metabolism
- Cell Survival/physiology
- Embryo, Nonmammalian/drug effects*
- Embryo, Nonmammalian/metabolism
- Glutathione Peroxidase/metabolism
- NF-E2-Related Factor 2/metabolism
- Oxidative Stress/drug effects*
- Photoreceptor Cells, Vertebrate/drug effects*
- Photoreceptor Cells, Vertebrate/metabolism
- Reactive Oxygen Species/metabolism
- Superoxide Dismutase/metabolism
- Superoxide Dismutase-1/metabolism
- Zebrafish/embryology*
- Zebrafish Proteins/metabolism
- PubMed
- 29928899 Full text @ Exp. Eye. Res.
Citation
Albalawi, A., Hasaballah A Alhasani, R., Biswas, L., Reilly, J., Akhtar, S., Shu, X. (2018) Carnosic acid attenuates acrylamide-induced retinal toxicity in zebrafish embryos. Experimental Eye Research. 175:103-114.
Abstract
Acrylamide (ACR) is a water-soluble chemical used widely in industry, which can be formed in tobacco smoke and in starchy foods cooked at high temperatures. ACR is considered to be a neurotoxin, genotoxin and carcinotoxin. Previous studies reported that ACR-exposed workers and experimental animals exhibited visual function defects, although the underlying mechanisms have not been elucidated. In this study, we found that zebrafish embryos exposed to 1 mM and 2 mM ACR showed significantly increased reactive oxygen species (ROS), decreased expression of the antioxidant genes Sod1, Sod2, Catalase, GPX1 and Nrf2, reduced activity of superoxide dismutase (SOD) and catalase, and elevated malondialdehyde (MDA), compared with control embryos. ACR exposure caused loss of both rod and cone photoreceptor cells through Caspase-3-dependent apoptotis. When embryos were simultaneously exposed to ACR and the natural antioxidative substance carnosic acid (CA), the presence of the latter (10 μM) markedly counteracted the above ACR-induced toxic effects. Our data suggest that CA can protect photoreceptor cells against ACR-induced oxidative damage and has a potential for neuroprotection of visual function in humans exposed to ACR.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping